Theory: AVNRT is a supraventricular tachycardia, which means that the arrythmia originates from either the atria or AV-node. A premature atrial complex (PAC) often luxates the arrythmia, as the consequential depolarisation wave can induce a re-entry circuit inside the AV-node (1). The AV-node contains two bundles: a slow pathway (alpha cells) and a fast pathway (beta cells). Almost always (~ 90%) the circle tachycardia arises within the slow pathway, resulting in retrograde activation of the atria through the fast pathway. Therefore, the typical AVNRT (or “slow-fast AVNRT”), the atrial contraction follows shortly after the ventricular contraction. This results in the P-wave showing during (invisible) or just shortly after the QRS-complex (short RP interval)! ---------
Clinic: Typically, AVNRT has a sudden onset of rapid regular palpitations which end just as sudden. The heartrate varies from 100-250 bpm – typically 180 bpm. The high frequency and therefore consequential release of natriuretic peptides (BNP) can lead to excessive urination: polyuria. Due to the often simultaneous contraction of the atria and the ventricles, the atria might contract against closed atrioventricular valves. In this case, the only way the blood of the right atria can flow is back into the inferior vena cava. This leads to strong venous ‘pulsations’ that can be visible in the neck – so called “cannon waves” sometimes even resulting in the “frog sign” (2).
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Case: The ECG shows characteristics of AVNRT, but with clear inverted P-waves - before - the QRS-complex in leads II, III and aVF (3). Indeed, the PR-interval is much longer than in typical AVNRT, but the P-wave effectively appears ‘before’ the QRS complex. This might be initially misleading, as the delayed retrograde atrial activation is in fact much slower: the rare (~ 6%) and atypical form of AVNTR! In other words: depolarisation of the atria has occurred much later than depolarisation of the ventricles.
Learn more about cardiology by Dr Boon Lim: https://drboonlim.co.uk
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